Pharmacological analysis of nod factor-induced calcium spiking in Medicago truncatula.: Evidence for the requirement of type IIA calcium pumps and phosphoinositide signaling

Pharmacological analysis of nod factor-induced calcium spiking in Medicago truncatula.: Evidence for the requirement of type IIA calcium pumps and phosphoinositide signaling
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DOI:
10.1104/pp.010691
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发表时间:
2002-04-01
期刊:
影响因子:
7.4
通讯作者:
Long, SR
Long, SR
中科院分区:
生物学1区
文献类型:
--
作者:
Engstrom, EM;Ehrhardt, DW;Long, SR

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细菌结瘤因子在相容的豆科植物宿主的根毛中触发许多细胞反应,其中包括细胞溶质钙水平的周期性、瞬时性增加,称为钙尖峰。我们筛选了13种真核细胞信号转导的药物调节剂对Nod因子诱导的钙离子尖峰的影响。该筛选的目的是双重的:涉及苜蓿属物种中结瘤因子诱导的钙尖峰所需的酶,并鉴定适合于将钙尖峰与其它结瘤因子反应相关联的钙尖峰抑制剂,从而开始理解钙尖峰在结瘤因子信号转导中的功能。2-氨基乙氧基二苯基硼酸盐、咖啡因、环匹阿尼酸(CPA)、2,5-二-(叔丁基)-1,4-氢醌和U-73122抑制Nod因子诱导的钙峰。CPA和U-73122分别是植物IIA型钙泵和磷脂酶C的抑制剂,并且暗示了在Nod因子诱导的钙尖峰中对这些酶的需要。CPA和U-73122在对根毛没有明显毒性的浓度下强烈抑制结瘤因子诱导的钙尖峰,使得CPA和U-73122适合于测试钙尖峰是否是随后的结瘤因子响应的原因。
Bacterial Nod factors trigger a number of cellular responses in root hairs of compatible legume hosts, which include periodic, transient increases in cytosolic calcium levels, termed calcium spiking. We screened 13 pharmaceutical modulators of eukaryotic signal transduction for effects on Nod factor-induced calcium spiking. The purpose of this screening was 2-fold: to implicate enzymes required for Nod factor-induced calcium spiking in Medicago sp., and to identify inhibitors of calcium spiking suitable for correlating calcium spiking to other Nod factor responses to begin to understand the function of calcium spiking in Nod factor signal transduction. 2-Aminoethoxydiphenylborate, caffeine, cyclopiazonic acid (CPA), 2,5-di-(t-butyl)-1,4-hydroquinone, and U-73122 inhibit Nod factor-induced calcium spiking. CPA and U-73122 are inhibitors of plant type IIA calcium pumps and phospholipase C, respectively, and implicate the requirement for these enzymes in Nod factor-induced calcium spiking. CPA and U-73122 inhibit Nod factor-induced calcium spiking robustly at concentrations with no apparent toxicity to root hairs, making CPA and U-73122 suitable for testing whether calcium spiking is causal to subsequent Nod factor responses.